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Aβ(31–35) and Aβ(25–35) fragments of amyloid beta‐protein induce cellular death through apoptotic signals: Role of the redox state of methionine‐35
Author(s) -
Clementi M. Elisabetta,
Marini Stefano,
Coletta Massimo,
Orsini Federica,
Giardina Bruno,
Misiti Francesco
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.04.041
Subject(s) - methionine , apoptosis , redox , microbiology and biotechnology , chemistry , programmed cell death , mitochondrion , amyloid (mycology) , biophysics , beta (programming language) , neurotoxicity , biochemistry , toxicity , biology , amino acid , inorganic chemistry , organic chemistry , computer science , programming language
Taken together our result indicate that Aβ(31–35) and Aβ(25–35) peptides in non‐aggregated form, i.e., predominantly monomeric, are strongly neurotoxic, having the ability to enter within the cells, determining mitochondrial damage with an evident trigger of apoptotic signals. Such a mechanism of toxicity seems to be dependent by the redox state of methionine‐35.